The DOI matches its Crossref record; 123 of the 124 references it cites were found in a registry or an index.
Aging and Genome Maintenance: Lessons from the Mouse?
Abstract
Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.
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“In addition to preventing cancer, genes that help maintain genomic integrity also prevent or retard the development of other aging phenotypes and age-related pathologies (Hasty et al., 2003).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Hasty et al., 2003
In the citing paper
“It is now apparent that many kinds of oncogenic or stressful stimuli can induce a senescence response. Foremost among these are certain types of DNA damage, including DNA breaks and oxidative lesions caused by environmental insults, genetic defects, or endogenous processes (DiLeonardo et al., 1994; Hasty et al., 2003; Samper et al., 2003).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Hasty et al., 2003
In the citing paper
“mutations in genes involved in this pathway do not produce aging manifestations: they are either lethal or confer no obvious phenotypes (Hasty et al., 2003”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Hasty et al., 2003
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Laminopathies and the long strange trip from basic cell biology to therapy
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“It is well documented that mice defective in mechanisms involved in the repair of oxidative DNA damage age faster and live shorter (Hasty et al., 2003).”
BackgroundGenetic mouse models of brain ageing and Alzheimer's disease
Bilkei‐Gorzó, A. (2013) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.12.009 · Cited by 253
A Life‐History Perspective on Short‐ and Long‐Term Consequences of Compensatory Growth
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“…occurs as a consequence of oxidative damage (e.g., Minakami and Fridovich 1990; Chatgilialoglu and O’Neill 2001; Karanjawala and Lieber 2004; Lu et al. 2004), and the maintenance of genome integrity is increasingly recognized as a major factor in longevity and cell viability (Hasty et al. 2003).”
BackgroundA review and appraisal of the DNA damage theory of ageing
Freitas, A. A., & de Magalhães, J. P. (2011) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2011.05.001 · Cited by 256
van der Pluijm, I., Garinis, G. A., Brandt, R. M. C., Gorgels, T. G. M. F., Wijnhoven, S., Diderich, K. E. M., de Wit, J., Mitchell, J. R., van Oostrom, C., Beems, R. B., et al. (2006) · PLoS Biology · doi:10.1371/journal.pbio.0050002 · Cited by 240
“]. These observations, together with the notion that DNA lesions can provoke a permanent cell cycle arrest or apoptosis, led us to propose that ageing can result from (oxidative) DNA lesions that interfere with transcription and/or replication causing cell death or cellular senescence, ultimately leading to the loss o…”
Self-citationTranscription — guarding the genome by sensing DNA damage
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“Although a responsive apoptotic pathway would efficiently remove damaged cells and therefore suppress carcinogenesis, such increased cell loss is thought to promote accelerated agein”
BackgroundKrishnan, V., Chow, M. Z. Y., Wang, Z., Zhang, L., Liu, B., Liu, X., & Zhou, Z. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1102789108 · Cited by 236
Relevance of the p53–MDM2 axis to aging
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Somatic mutations in aging, cancer and neurodegeneration
Kennedy, S. R., Loeb, L. A., & Herr, A. J. (2011) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2011.10.009 · Cited by 223
“A number of mouse lines that are deficient in DNA damage repair show an aging phenotype, and also exhibit increased rates of cancer (Hasty et al., 2003).”
BackgroundTelomere Shortening Exposes Functions for the Mouse Werner and Bloom Syndrome Genes
Du, X., Shen, J., Kugan, N., Furth, E. E., Lombard, D. B., Cheung, C., Pak, S., Luo, G., Pignolo, R. J., DePinho, R. A., et al. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.19.8437-8446.2004 · Cited by 213
Delayed and Accelerated Aging Share Common Longevity Assurance Mechanisms
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“invaluable for studying accelerated aging [1].”
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Self-citationDelayed kinetics of DNA double‐strand break processing in normal and pathological aging
Sedelnikova, O. A., Horikawa, I., Redon, C., Nakamura, A., Zimonjic, D. B., Popescu, N. C., & Bonner, W. M. (2008) · Aging Cell · doi:10.1111/j.1474-9726.2007.00354.x · Cited by 207
Controlling the subcellular localization of DNA polymerases ι and η via interactions with ubiquitin
Plosky, B. S., Vidal, A. E., de Henestrosa, A. R. F., McLenigan, M. P., McDonald, J. P., Mead, S., & Woodgate, R. (2006) · The EMBO Journal · doi:10.1038/sj.emboj.7601178 · Cited by 201
“In human cells, nucleotide excision repair (NER) removes most UV-induced DNA damage before replication takes place (Hoeijmakers, 2001; Hasty et al, 2003).”
BackgroundMolecular bases of progeroid syndromes
Navarro, C. L., Cau, P., & Lévy, N. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl214 · Cited by 189
Sun, L.-Q., Lee, D. W., Zhang, Q., Xiao, W., Raabe, E. H., Meeker, A. K., Miao, D., Huso, D. L., & Arceci, R. J. (2004) · Genes & Development · doi:10.1101/gad.1176104 · Cited by 186
“Genome instability in patients with Werner syndrome, due to mutations in the WRN DNA helicase, is associated with early onset of aging and cancer predisposition (Hasty et al. 2003).”
BackgroundInfluentialWhat Can Progeroid Syndromes Tell Us About Human Aging?
Kipling, D., Davis, T., Ostler, E. L., & Faragher, R. (2004) · Science · doi:10.1126/science.1102587 · Cited by 184
The mouse as a model organism in aging research: Usefulness, pitfalls and possibilities
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“Cancer is a disease that generally affects most mammalian species and is usually believed to be an unavoidable accompaniment of aging (Campisi, 2003; Hasty et al., 2003; Lombard et al., 2005).”
BackgroundEarly aging–associated phenotypes in Bub3/Rae1 haploinsufficient mice
Baker, D. J., Jeganathan, K. B., Malureanu, L., Perez-Terzic, C., Terzic, A., & van Deursen, J. M. A. (2006) · The Journal of Cell Biology · doi:10.1083/jcb.200507081 · Cited by 175
Aging, tumor suppression and cancer: high wire-act!
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“These damaged cells may contribute to the age-related decline in tissue function because deficiencies in DNA repair can accelerate aging phenotypes (Hasty et al., 2003), the DNA damage that accumulates with age in hematopoietic stem cells greatly limits their function (Nijnik et al., 2007; Rossi et…”
BackgroundSelf-citationDNA Repair Defects in Stem Cell Function and Aging
Park, Y., & Gerson, S. L. (2004) · Annual Review of Medicine · doi:10.1146/annurev.med.56.082103.104546 · Cited by 172
Nuclear envelope defects cause stem cell dysfunction in premature-aging mice
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The critical roles of somatic mutations and environmental tumor-promoting agents in cancer risk
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Systems biology of ageing and longevity
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Rodents for comparative aging studies: from mice to beavers
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“In gerontological research, the first mammalian mutants with altered lifespan were generated in mice (reviewed in Hasty et al. 2003; Bartke and Brown-Borg 2004; Hasty and Vijg 2004), and mice and rats were the first mammals to reveal the life-prolonging”
BackgroundFunctional dysregulation of stem cells during aging: a focus on skeletal muscle stem cells
García‐Prat, L., Sousa‐Victor, P., & Muñoz‐Cánoves, P. (2013) · The FEBS Journal · doi:10.1111/febs.12221 · Cited by 152
Deletion of Ku70, Ku80, or Both Causes Early Aging without Substantially Increased Cancer
Li, H., Vogel, H. S., Holcomb, V. B., Gu, Y., & Hasty, P. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.00785-07 · Cited by 158
“This is certainly true for many of the models of accelerated aging in humans like Werner’s syndrome and Hutchinson-Gilford syndrome ( 25 , 37).”
BackgroundSelf-citationNucleotide excision repair: new tricks with old bricks
Kamileri, I., Karakasilioti, I., & Garinis, G. A. (2012) · Trends in Genetics · doi:10.1016/j.tig.2012.06.004 · Cited by 146
SIRT6 in DNA repair, metabolism and ageing
Lombard, D. B., Schwer, B., Alt, F. W., & Mostoslavsky, R. (2008) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2007.01902.x · Cited by 148
Genotype–phenotype correlations in Fanconi anemia
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“These data demonstrate that DNA damage and/or tumor suppressor gene mutation causes tumor formation and/or premature aging (Vijg and Dolle, 2002; Campisi, 2003; Hasty et al, 2003).”
BackgroundThe short-lived African turquoise killifish: an emerging experimental model for ageing
Kim, Y., Nam, H. G., & Valenzano, D. R. (2016) · Disease Models & Mechanisms · doi:10.1242/dmm.023226 · Cited by 146
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Methusaleh's Zoo: How Nature provides us with Clues for Extending Human Health Span
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“These mice are invariably short-lived and exhibit some signs of accelerated ageing (Hasty et al., 2003).”
Premature aging in mice activates a systemic metabolic response involving autophagy induction
Mariño, G., Ugalde, A. P., Salvador-Montoliu, N., Varela, I., Quirós, P. M., Cadiñanos, J., van der Pluijm, I., Freije, J. M. P., & López-Otı́n, C. (2008) · Human Molecular Genetics · doi:10.1093/hmg/ddn120 · Cited by 144
“Recently, several studies have demonstrated that the nuclear envelope abnormalities that lead to accelerated aging may also contribute to normal aging (23,24), supporting the idea that the laboratory-engineered progeroid models are useful tools for studying the mechanisms underlying normal aging (25).”
BackgroundThe oxidative DNA lesions 8,5′-cyclopurines accumulate with aging in a tissue-specific manner
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Genetics of Longevity and Aging
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Metadata
- Authors
- Hasty, P., Campisi, J., Hoeijmakers, J., van Steeg, H., & Vijg, J.
- Affiliations
- Department of Molecular Medicine,
- Buck Institute for Research on Aging (US)
- Erasmus University Rotterdam (NL)
- National Institute of Public Health and the Environment, Post Office Box 1, 3720 BA Bilthoven, Netherlands.
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Hasty, Paul
- Vijg, Jan
- Venue
- Science
- Published
- 2003-02-28
- Volume
- 299
- Issue
- 5611
- Pages
- 1355-1359
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2133469432
- Cited by
- 553
- References
- 124
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 7 · 2023: 12 · 2022: 12 · 2021: 10 · 2020: 14 · 2019: 15 · 2018: 13 · 2017: 8 · 2016: 25 · 2015: 18 · 2014: 27 · 2013: 29 · 2012: 32
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Rivm Repository (Netherlands National Institute for Public Health and the Environment) (submittedVersion)
- Funders
- National Institute on Aging (AG 17242, P01AG017242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- aging, genome maintenance, genome stability, mouse model, longevity, somatic maintenance, energy metabolism, DNA damage, model organisms, human aging
- MeSH terms
- Werner Syndrome Helicase, Aging, Animals, DNA Damage, DNA Repair, DNA Helicases, Exodeoxyribonucleases, Humans, Longevity, Mutation, Syndrome, Transcription, Genetic, Genome, Human, Telomere, Genome, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Aging, Premature, Mice, RecQ Helicases
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